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Biomedical subjects

A M Scher

Publications and source records attributed to A M Scher.

At least 19 recordsLinked to original sources
PubMed1992

Recovery of arterial pressure control after partial baroreceptor denervation in awake rabbits.

We examined recovery of control of heart rate (HR) and total peripheral resistance (TPR) by arterial baroreceptors after bilateral carotid sinus and aortic denervation or unilateral carotid sinus and aortic denervation in conscious rabbits. In one group of animals, HR responses to changes in mean arterial pressure (MAP) after injection of nitroglycerin or phenylephrine were measured in control studies and at 2, 5, 10, and 15 days after partial baroreceptor denervation. All denervation procedures increased MAP and HR at 2 and 5 days after denervation. Reflex sensitivity decreased to 57-67% of control on day 2 after denervation. HR responses recovered by day 10 after bilateral aortic or carotid sinus denervation; however, recovery following unilateral denervation was less complete. In a second group of animals, studied after implantation of aortic flowmeters, TPR changes following reduction in cardiac output by inferior vena caval occlusion were 49% of control responses on day 2 after denervation and returned close to control level on day 5. Controls of HR and TPR recovered substantially and were not significantly different from control 10 days after partial denervation. Recovery apparently occurred through the remaining arterial baroreceptors, possibly due to central reorganization of reflex pathways.

Animals↗
PubMed1991

Baroreflex-induced vasoconstriction in active skeletal muscle of conscious dogs.

We investigated the magnitude of baroreflex-mediated vasoconstriction in the hindlimbs of six conscious dogs at rest and during four levels of treadmill exercise ranging in intensity from mild (2 mph, 0% grade) to heavy (6 mph, 10% grade). Dogs were instrumented with vascular occluders on both common carotid arteries, an electromagnetic flow probe and vascular occluder on the terminal aorta, and a catheter in a branch of the femoral artery; aortic baroreceptors were intact. The responses to a 2-min carotid occlusion were observed at rest and after 3-5 min of exercise at each work rate. The increases in mean arterial pressure during carotid occlusion were similar at rest and at each level of exercise (26 +/- 4 to 35 +/- 3 mmHg; no significant difference). At rest, carotid occlusion caused only a small but significant decrease in terminal aortic vascular conductance (TAC) (-0.89 +/- 0.21 ml.min-1.mmHg-1, P less than 0.05). During mild exercise, baseline terminal aortic blood flow (TAQ) and TAC increased, and the reduction in TAC during carotid occlusion exceeded that observed at rest (-1.85 +/- 0.42 ml.min-1.mmHg-1, P less than 0.05). As exercise intensity increased, the magnitude of the reduction in TAC during carotid occlusion increased linearly with the baseline TAQ. At the highest work rate, approximately 59% of the increase in mean arterial pressure during carotid occlusion was due to the large decrease in TAC (-6.35 +/- 0.50 ml.min-1.mmHg-1). We conclude that the vasoconstriction of active skeletal muscle during the pressor response to bilateral carotid occlusion increased with exercise intensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Time course of recovery of arterial pressure control after carotid denervation.

We examined the recovery of arterial pressure control after carotid sinus baroreceptor denervation in conscious dogs with atrioventricular block. Strength of control was assessed by measuring changes in peripheral resistance and atrial rate after step changes in cardiac output. One day after carotid denervation, arterial pressure was significantly elevated (+13.7 mmHg), and the strength of control of peripheral resistance and atrial rate were significantly decreased to 46.1 and 36.6% of control, respectively. Over 4-7 days, the strength of control of both peripheral resistance and atrial rate and the mean arterial pressure returned to the levels observed before denervation. After carotid denervation, the pressor response to bilateral carotid artery occlusion was abolished, and thus the recovery of arterial pressure control was not caused by inadequate carotid denervation or regeneration of carotid baroreceptors. The recovery of arterial pressure control after carotid denervation is probably caused by an increase in the reflex responses to pressure changes at the aortic baroreceptors and may reflect plasticity within the baroreflex pathway.

Animals↗
PubMed1990

Pulsatile pressure can prevent rapid baroreflex resetting.

In a previous study [Am. J. Physiol. 255 (Heart Circ. Physiol. 24): H673-H678, 1988] we demonstrated that baroreflex responses decay (reset) to increased static sinus pressures, but with increased pulsatile pressure, responses are maintained. To determine more conclusively whether pulsatile pressure prevents rapid baroreflex resetting in this study we examined resetting as shifts of the baroreflex (sinus pressure-arterial pressure) curve. In seven anesthesized rabbits the left sinus was vascularly isolated and conditioned for 5 min to static or pulsatile pressures of 60, 100, or 140 mmHg mean pressure, 0 or 35-40 mmHg pulse pressure. The baroreflex curve was then determined by stepwise changing sinus pressure from 40 to 160 mmHg in 20-mmHg increments. Threshold, midpoint, and saturation sinus pressures shifted 25-39% with static conditioning pressures but did not shift significantly with pulsatile pressures. Also, the baroreflex responses to step increases in static sinus pressure decayed, as resetting occurred, but did not decay with pulsatile sinus pressure increases. Thus the baroreflex rapidly resets with static pressures, but there is minimal, if any, resetting with pulsatile pressures.

Animals↗
PubMed1990

Baroreflex attenuates pressor response to graded muscle ischemia in exercising dogs.

Graded reductions in hindlimb perfusion in dogs exercising at 2 miles/h (0% grade) elicited reflex pressor responses by what is referred to as the "muscle chemoreflex." To determine the extent to which arterial baroreceptor reflexes oppose the muscle chemoreflex, we elicited pressor responses to muscle ischemia before and after chronic surgical denervation of the arterial baroreceptors. The muscle chemoreflex showed a threshold beyond which systemic pressure rose approximately 3 mmHg for each 1-mmHg decrease in hindlimb perfusion pressure when the arterial baroreceptors were intact. Arterial baroreceptor denervation approximately doubled the pressor responses, i.e., systemic pressure rose by approximately 6 mmHg for each 1-mmHg fall in hindlimb perfusion pressure, without alteration in threshold. We conclude that during mild dynamic exercise, the arterial baroreflexes oppose the pressor response to graded reductions in hindlimb perfusion, reducing it by approximately 50%. When unopposed by the arterial baroreflexes the muscle chemoreflex exhibits a gain (ratio of change in systemic pressure to change in hindlimb perfusion pressure) of approximately -6; thus this reflex can correct by 85% the decrease in muscle perfusion pressure caused by partial vascular occlusion.

Animals↗
PubMed1989

Effects of steps in cardiac output and arterial pressure in awake dogs with AV block.

In awake dogs with atrioventricular block, we examined the responses in total peripheral resistance and atrial rate to square-wave changes in mean arterial pressure or cardiac output. We compared the responses 2-3 min after a step change with the responses 19-20 min after a step. With resetting of arterial pressure control, the compensatory responses should decrease as the baroreceptors reset to the prevailing pressure. With step changes in mean arterial pressure or cardiac output, the responses in both peripheral resistance and atrial rate increased from minutes 2-3 to minutes 19-20. The responses in peripheral resistance also increased in animals studied after bilateral vagal block. All of the above changes were significant in the majority of cases. In another experiment, the animals were "conditioned" by 20 min at imposed high or low pressure. When control was returned to the animal after conditioning at high pressure, arterial pressure was not significantly different (P greater than 0.05) from the initial control levels. When control was returned after conditioning at low pressure, arterial pressure was significantly greater (P less than 0.05) than during the initial control period. These results indicate an absence of resetting of the entire arterial pressure control system.

Animals↗
PubMed1989

Cardiovascular control by arterial and cardiopulmonary baroreceptors in awake dogs with atrioventricular block.

We studied reflex responses to pressure changes at arterial and cardiopulmonary baroreceptors in five awake dogs with atrioventricular block before and after baroreceptor denervation. We changed ventricular pacing rate and blood volume to vary cardiac output and arterial (MAP) and central venous pressure (CVP). We determined peripheral resistance (TPR) and atrial rate (HRA) as responses. In the intact animal, regression analysis showed an average relationship across dogs of TPR = 169-0.69 MAP-1.952 CVP + error. Correlation (r) between observed and predicted TPR was 0.83. For HRA, regression indicated HRA = 291.66-2.319 MAP + 8.144 CVP + error (r = 0.899). TPR and MAP are percent of control at 90 beats/min; CVP is in mmHg; HRA, in beats/min. Although its coefficient is smaller, MAP explains approximately 69% of the variation in TPR. After arterial baroreceptor denervation, effects of MAP on TPR were insignificant and the coefficient for CVP increased. Subsequent vagal block eliminated all reflex responses. Effects from the two receptor sites sum linearly. They act cooperatively with changes in blood volume, but oppose one another with cardiac output changes.

Animals↗
PubMed1988

Pulsatile sinus pressure changes evoke sustained baroreflex responses in awake dogs.

A modified Stephenson-Donald preparation was used to control pressure in an isolated carotid sinus in conscious dogs with all other arterial baroreceptors denervated. Sinus pressure was changed from preisolation control levels to either an elevated static or an elevated pulsatile pressure for 5 min. These sinus pressure changes evoked similar initial decreases in arterial pressure. The elevated static sinus pressure (150 or 175 mmHg) caused an initial depressor response of -32.7 +/- 5.5 mmHg, which then decayed rapidly. Five minutes after the change in sinus pressure, the depressor response was abolished, as arterial pressure returned to control pressure. This decay of the response would be expected if resetting occurred. In contrast, when the sinus was exposed to elevated pulsatile pressures (125 or 150 mmHg mean, 50 mmHg pulse pressure) depressor responses were sustained throughout the sinus pressure change (-23.2 +/- 5.3 mmHg initial, -29.0 +/- 4.8 mmHg at 5 min; P greater than 0.4). These results demonstrate that while the reflex responses rapidly reset to elevated static sinus pressures, elevated pulsatile pressures elicit sustained reflex responses.

Animals↗
PubMed1988

Arterial pressure control after chronic carotid sinus denervation.

This study examines the control of arterial blood pressure in conscious, instrumented dogs with atrioventricular block before and greater than or equal to 9 days after carotid sinus baroreceptor denervation. Strength of reflex control of blood pressure was quantitated by measuring the changes in peripheral resistance and atrial rate after square wave changes in cardiac output. Surprisingly, nine or more days after carotid denervation, the strength of baroreflex control of peripheral resistance and atrial rate were not different (P greater than 0.05) from the values before denervation. This was not due to a change in the base-line levels of arterial pressure, atrial rate, cardiac output, or peripheral resistance. Bilateral vagal block after carotid denervation removed reflex effects from remaining baroreceptors and virtually eliminated changes in peripheral resistance in response to changes in arterial pressure. Therefore, the compensatory responses observed after carotid denervation were mediated by the remaining baroreceptors. Thus, after chronic carotid sinus denervation, there is no decrease in the strength of baroreflex control of peripheral resistance or heart rate.

Animals↗
PubMed1987

Does inadequate oxygen delivery trigger pressor response to muscle hypoperfusion during exercise?

In dogs running on a treadmill at 2 or 4 mph or 4 mph plus 10% incline, graded reductions in hindlimb perfusion reflexly elicited pressor responses. To test the idea that systemic arterial pressure (SAP) is raised by accumulation in muscle of a nerve-activating "pressor substance" release when O2 delivery becomes inadequate, arterial O2 content (CaO2) was reduced 29.1% by carbon monoxide (CO) inhalation before repeating exercise at 2 mph. We reasoned that the pressor substance, or related substances, should appear in femoral venous blood and be correlated to SAP. [K+] behaved inappropriately as a signal to raise SAP, i.e., when flow was reduced, SAP rose markedly with little or no change in [K+]. SAP was well correlated to pH and [lactate] over the three work loads. Compared with the same work load with normal CaO2, CO shifted the relation between SAP and terminal aortic flow rightward 0.30 l/min (34.5%) and the relation between SAP and PO2 leftward 7.7 mmHg. CO did not affect the relation of SAP to terminal aortic O2 delivery, hindlimb O2 uptake index, pH, or [lactate]. Thus pressor responses are apparently generated when O2 delivery falls below some critical level causing accumulation of a pressor substance the release of which is linked to a metabolic event that precipitates lactate accumulation.

Animals↗
PubMed1986

The nature of the exercise stimulus.

The two foremost hypotheses concerning the nature of the exercise stimulus are: Central Command. Centrally generated signals activate in parallel cardiovascular and skeletal muscle motor systems; Muscle Chemoreflex. Chemosensitive nerves within the skeletal muscle detect local accumulations of metabolites which reflect disparities between muscle blood flow and metabolism. The focus is mainly on the second hypothesis. The neurophysiological basis for this reflex is well established. Accumulations of metabolites within ischemic muscle reflexly trigger pressor responses that are abolished by blockade of sensory nerves from muscle. However, such blockade does not abolish circulatory responses to static or mild dynamic exercise. To assess the importance of muscle chemoreflexes, stepwise partial occlusions of the terminal aorta were made in exercising dogs. The rise in arterial pressure was related to reductions in terminal aortic flow and arterial pressure below the occluder. In mild exercise sensitivity of the reflex was low until flow was substantially reduced to a threshold. In heavier exercise sensitivity of the reflex was high (no threshold) and could provide a tonically active exercise stimulus. The nature of the metabolic signal is unknown. The pressor response was most closely related to femoral venous lactate concentration and unrelated to femoral venous K+ or PO2.

Animals↗
PubMed1985

The control of atrial contraction by ventriculo-atrial pacing in the dog with AV block.

Atrial contraction in dogs with atrioventricular (AV) block was controlled by multiple atrial stimuli delivered during ventricular diastole. Acute hemodynamic changes were assessed. At a ventricular rate of 60 bpm, the spontaneous atrial rate averaged 83, and atrial cannon waves were frequent. When the atria were given two stimuli at an interval of 500 ms during ventricular diastole, the cannon waves were eliminated completely, and a fall in mean central venous pressure and a rise in systemic blood pressure were found. At a pacing rate of 90 bpm, similar changes in the cannon waves, mean central venous pressure, and systemic blood pressure were found when two atrial stimuli followed ventricular stimulation. Ventriculo-atrial multiple pacing may be useful in both clinical and experimental AV block.

Animals↗
PubMed1984

Long-term responses of atrial rate and peripheral resistance to changes in ventricular pacing rate in awake dogs with atrioventricular block.

We wished to see if a maintained change in pressure at the baroreceptors leads to a maintained or a transient change in heart rate and total peripheral resistance, and if long-term changes in rate and resistance paralleled one another. In awake dogs with intact baroreceptors and complete atrioventricular block, ventricular rate was held alternately at high (90 beats/min) and low (50 beats/min) levels, each for 2 days. This cycle was repeated several times. Data were recorded for 1.5 hours each day. With this change in ventricular rate, there was a maintained change over 2 days in arterial (14.4 +/- 1.0 mm Hg) and central venous (3.0 +/- 1.2 mm Hg) pressures. These changes in pressure were accompanied by a maintained change in atrial rate of 41.1 +/- 9.4 beats/min; peripheral resistance, however, changed only transiently. In three animals, the half-cycle length was 1 week. Changes in heart rate also persisted for this period. It appears from these studies that there is long-term control of heart rate, but not of peripheral resistance. Hypotheses to explain these results are presented.

Animals↗
PubMed1984

Changes in vascular capacity in awake dogs in response to carotid sinus occlusion and administration of catecholamines.

Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and beta-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1-2.0 micrograms/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03-0.51 micrograms/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01-0.40 micrograms/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 +/- 0.6 ml/mm Hg per kg. In the conscious, resting dog, both alpha- and beta-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The beta-adrenergic responses predominate.

Animals↗
PubMed1983

Cardiovascular responses to graded reductions in hindlimb perfusion in exercising dogs.

In six dogs trained to run at 2, 4, and 6 mph, we caused graded reductions in hindlimb perfusion by compressing the terminal aorta. Our goal was to examine the relationship between hindlimb perfusion [terminal aortic flow (TAQ) and femoral arterial pressure (FP)] and cardiovascular responses [aortic pressure (AP), heart rate, and ascending aortic flow (CO)]. Small reductions in TAQ and FP produced bradycardia, small decreases in CO, and small increases in AP. Further reductions in TAQ and FP produced tachycardia, increased CO, and large increases in AP. AP rose by about 1 mmHg for each 1-mmHg fall in FP. The response was similar at all speeds, but as work load increased it required smaller reductions in FP and TAQ to cause a pressor response (e.g., at 6 mph we could not demonstrate a nonlinear relationship between TAQ and AP). At low work loads the cardiovascular responses to exercise were most likely set by signals other than feedback from exercising muscle because substantial reductions in hindlimb perfusion caused no significant cardiovascular responses. At moderate-to-high work loads or where muscle perfusion is restricted, metabolic feedback from muscle may play a role in cardiovascular responses to exercise.

Animals↗
PubMed1983

Angiotensin causes vasoconstriction during hemorrhage in baroreceptor-denervated dogs.

The participation of angiotensin II (ANG II) in the maintenance of arterial blood pressure during hypotensive hemorrhage was examined in unanesthetized, baroreceptor-denervated dogs. When mean aortic blood pressure was reduced to 69.0 +/- 2.2 mmHg, plasma renin activity increased from 0.6 +/- 0.3 ng ANG I X ml-1 X h-1 during the prehemorrhage control period to 4.5 +/- 1.6. Twenty minutes after the hemorrhage, mean aortic blood pressure rose to 78.9 +/- 3.1 mmHg. Subsequent infusion of the angiotensin II antagonist saralasin (5.2-14.0 micrograms X kg-1 X min-1) decreased mean aortic pressure to 59.6 +/- 3.3 mmHg. When 5% dextrose was infused in place of saralasin, mean aortic pressure was 79.3 +/- 4.3 mmHg. The lower aortic blood pressure caused by saralasin infusion was the result of a significant decrease in total peripheral resistance. Resistance was 10.3 +/- 3.2 mmHg X l-1 X min lower during saralasin infusion than during dextrose infusion. We conclude that baroreceptor reflexes are not essential for the elevation of plasma renin activity during hemorrhage. In baroreceptor-denervated dogs subjected to hypotensive hemorrhage, the increased formation of ANG II has a vasoconstrictor action that contributes to the maintenance of arterial blood pressure.

Angiotensin II↗
PubMed1982

Beat-by-beat control of cardiac output in awake dogs with atrioventricular block.

In dogs with atrioventricular block and implanted ascending aortic flow probes, cardiac output can be controlled on each beta. The procedure is implemented through on-line use of a digital computer. The algorithm has three steps: 1) aortic flow is measured and integrated to give stroke volume; 2) at the end of ejection, the program computes how long the current beat must be to keep cardiac output at a target level; and 3) the ventricle is stimulated at the proper time. Cardiac output can be controlled over a range of 60-110% of normal in a resting dog. This range can be expanded by combining hemorrhage or volume infusion with the control procedure.

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